Mid-zone intramural arterial hypoxia has been implicatd indirectly as one of the factors involved in the maturation and degeneration of the atherosclerotic lesion, but has not been demonstrated conclusively under any condition. If it occurs, it appears that it should be found when an original process produces intimal or subintimal thickening which increases the diffusional distance for oxygen to the mid-layers of the avascular zone and/or alters the diffusion coefficient of oxygen utilization in a detrimental manner. Evidence suggests it may depend also on density and penetration of vasa vasorum. We propose to create standard intimal injury in two groups of animals: one (dog) found to have an extensive vasal system and the other (rabbit) thought to be deficient in vasal supply. At seven and 14 days, profiles of intramural oxygen tension will be obtained by a microcathode technique which does not lead to artifactual vascular deformation in vivo and has had extensive validation in this laboratory. Arterial geometry and vasal penetration will be measured at the sites of study by histologic techniques and examied in relation to lowest intramural pO2, vasal density, penetration, and avascular layer thickness. Contralateral uninjured arteries serve as additional controls.